This invention relates to transcutaneous nerve stimulation and more particularly to a transcutaneous nerve stimulating device which represents an advancement in the treatment of sympathetic nerve dysfunction. This invention is directed to the providing of a transcutaneous nerve stimulator which is designed to be utilized in T.E.N.S. (Transcutaneous Electrical Nerve Stimulation) therapy. T.E.N.S. therapy is based on a non-invasive, non-narcotic concept of pain management which is non-addictive, is not subject to abuse, and does not interact with drugs. T.E.N.S. therapy has already proven to be an effective modality in treating the organic pain problems associated with the following conditions involving the central nervous system: chronic lumbar and cervical strains or sprains, degenerating disc disease, degenerative arthritic disease, neuropathies, neuralgias, post-lumbar laminectomy syndrome, post-thoracotomy syndrome, bursitis, postphlebitis syndrome, phantom limb syndrome, and tension and migraine headaches.
Early attempts to suppress organic pain and other neurophysical effects utilizing electrical stimulation occurred as early as 2,000 years ago when it was discovered that gout apparently could be successfully treated by placing the diseased extremities in a tub of water filled with electric eels. Later, headaches were treated using a similar approach. A detailed, scientific investigation was finally conducted by Professor Galvani of the University of Bologna, which investigation is credited with ultimately leading to the development in the 1800's of electrical equipment for suppression of organic pain associated with the central nervous system. The earliest therapeutic devices utilizing electrical stimulation for the most part featured a constant amplitude and rate. Examples of the early art are Benz, U.S. Pat. No. 646,793; Raymond et. al., U.S. Pat. No. 872,148; Tibbals, U.S. Pat. No. 1,059,090; and Call, U.S. Pat. No. 1,908,688. A major problem with electrical stimulation therapy has been accommodation, whereby the nerve being stimulated in effect accommodates itself over time to the electrical charge, such that the effectiveness of the treatment is diminished.
It took scientists a long time to discover and attempt to address the problem. Nemec, U.S. Pat. No. 2,622,601; DiPerma, U.S. Pat. No. 2,624,342; and Gratzl, U.S. Pat. No. 2,771,554 all disclose electrotherapeutic devices with at least one including means to vary the rate, amplitude or pulse width of the generated electrical pulse. However, merely being able to change either the rate, amplitude or pulse width still resulted at best in an individual having to manually adjust the controls prior to the occurrence of accommodation. The process was both labor intensive and inefficient, with respect to the quality of the therapy, since maximum pain relief for the central nervous system was not being provided.
In 1967, a Dr. Sweet at Massachusetts General Hospital developed the first T.E.N.S. unit. The effectiveness of T.E.N.S. therapy is believed to be based on its incorporating two major pain control theories. Under the so-called Gate Control theory, pain can be inhibited and suppressed by "closing the gate" on pain signals. This theory postulates that by providing electrical stimulation of a sufficiently high pulse amplitude, narrow pulse width and high pulse rate the electrical signals race up large myelinated fibers faster than the pain signals travel up smaller unmyelinated fibers. The neural impulses transmitting pain information to the brain thus become interrupted, and since the brain fails to receive the pain signals, no pain is perceived. The other theory incorporated in T.E.N.S. units is the Endorphin Theory, also known as the Endogenous Opiate Theory. This theory postulates that the sustained input of T.E.N.S. signals triggers the release of naturally occurring pain making endorphins and enkephalins (morphine-like substances). These natural substances block pain signals by a mechanism of binding to receptors in the brain where pain perception occurs and inhibit pain information from reaching the brain.
There is a known clinical correlation between amplitude and pulse width with regard to the efficacy of the stimulus. As one shortens the duration of a pulse, its amplitude must be increased to maintain the efficacy of the stimulus. This relationship when plotted graphically is known as a strength-duration curve. Thus not only must the ideal T.E.N.S. units have adjustable amplitude and pulse width, but it must also be able to modulate those values in such a way as to approximate the strength-duration curve in the maximum sensory threshold.
This explains the shortcomings in Reiner, U.S. Pat. No. 2,808,826 which disclosed a unit which permitted instantaneous changes in pulse width and amplitude to two pre-set points along the strength-duration curve, and Maurer, U.S. Pat. No. 4,340,063 which disclosed a unit having its amplitude modulate in response to modulations in pulse width so as to approximate a portion of the strength-duration curve. The rate in Maurer was manually adjustable, but only to the extent taught by Miller, U.S. Pat. No. 4,084,595.
The problem with accommodation in the treatment of pain associated with the central nervous system was addressed in Spanton et al, U.S. Ser. No. 936,828, now U.S. Pat. No. 4,759,368. That particular device constituted an advancement in treatment of organic pain associated solely with the central nervous system. However, studies have shown that between 80 and 90% of chronic and acute pain involves sympathetic nerve dysfunction, and that in fact sympathetic nerve dysfunction constitutes between 10 and 80% of the actual problem. Sympathetic nerve dysfunction involves treating of the autonomic nervous system.
The sympathetic nervous system is part of the automatic network primarily responsible for vasoconstriction of arterial beds (i.e., the increase or decrease of blood flow in specific areas). This network controls arterial blood pressure, gastrointestinal mobility secretions, urinary output, sweating, body temperature regulation and artery blood flow. This system is comprised of pre- and post-ganglionic fibers and is involved either directly or indirectly in most chronic pain patients. In cases of sympathetic nerve dysfunction such as causalgia or non-specific lumbar or thoracic sympathetic dysfunction, these fibers are the primary causative agent. With many chronic pain patients, the sympathetic nervous system establishes an inhibitory reflex of vasoconstriction in the injured area resulting in hypoxemia. This lack of oxygen prevents adequate healing and in fact increases the pain in that area. It has only been within the past ten years that physicians have found that some relief for sympathetic nerve dysfunction can be obtained through T.E.N.S. treatment with a low frequency of pulsation, since sympathetic nerves have a repolarization time of 0.3 to 1.3 milliseconds.
Although physicians believe T.E.N.S. may be helpful in treating sympathetic nerve dysfunction, an unsolved problem relates to the amount of actual treatment time available using existing T.E.N.S. units. For example, it has not been uncommon to treat an individual for sympathetic nerve dysfunction for a period of five to ten minutes using low frequency burst pulsation with a therapist or doctor present. However, at the end of that time period, the amount of pain associated with the central nervous system and the patient's nociceptors is such that the patient must undergo treatment for perhaps the next four hours using high frequency pulsation to address central nervous system pain. Thus, after an extended period of time of T.E.N.S. treatment, the patient has only had a few minutes which actually addressed sympathetic nerve dysfunction with treatment of the sympathetic nerves occurring for less than 5% of the T.E.N.S. treatment time. One could not address problems of the autonomic and central nervous systems simultaneously.
Patients who tried to constantly, manually switch modes in an attempt to overcome the problem usually sacrificed maximum pain relief to either the autonomic or central nervous system. Plus the constant switching had to be prolonged for several hours for the treatment to even be nominally effective. Thus, prior devices and medical techniques have been extremely inefficient, despite the severity of the problem and the longfelt need.
Furthermore, the slow response time of the sympathetic nervous system precludes CNS strength-duration modulation with its high rates and relatively narrow widths. Thus treatment of sympathetic nerve dysfunction with traditional CNS strength-duration modulation does not result in the patient obtaining adequate pain relief.
Therefore, due to the problems associated with the treatment of sympathetic nerve dysfunction by T.E.N.S. therapy, the traditional medical approach has been to treat the sympathetic nervous system with various medications, including sympatholectyic drugs and various sympathomimetric drugs. These types of drugs have significant side effects either directly on the central nervous system or on generalized sympathetic functions, such as increased blood pressure or tachycardia. Thus, current approaches to treatment of sympathetic nerve dysfunction are either inefficient or entail significant physiological and pharmacologic side reactions. Therefore it is apparent that the need exists for an improved T.E.N.S. unit and methodology of treatment.